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Results for “Transient ischemic attack”

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PubMed2000

Lesions visualized by contrast-enhanced magnetic resonance imaging in transient ischemic attacks.

In patients with transient ischemic attacks (TIAs), contrast-enhanced magnetic resonance imaging (MRI) is more sensitive to visualize the recent ischemic lesions than conventional MRI. We examined the clinical characteristics of TIA patients presenting with enhanced lesions visualized by contrast-enhanced MRI. We retrospectively evaluated 64 patients with carotid TIAs. We evaluated the frequency and topography of TIA associated infarcts on contrast-enhanced MRI and compared the clinical background of patients with and without such lesions. Twenty-three patients underwent plain MRI only, while the remaining 41 patients underwent contrast-enhanced MRI. Of the latter 41 patients, 16 had abnormal enhanced lesions (39%: group L), while 25 had no lesions (61%: group NL). In group L, all lesions were spotty, and they were located in the cerebral cortex in 13 patients (81%), the subcortex in two (12%), and the perforator territory in one (6%). Aphasia or confusional state, hypertension, and emboligenic cardiac or arterial disease (stenosis > or =50%) were more frequently observed in group L than in group NL (38 vs. 8%, 81 vs. 48%, and 93 vs. 60%, respectively, P<0. 05). The TIA patients with enhanced lesions on MRI may be associated with an emboligenic cardiac or arterial disease, severe neurologic symptom compared to those without them.

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PubMed1976

Use of the Holter electrocardiographic monitor in the diagnosis of transient ischemic attacks.

The diagnosis of transient ischemic attacks usually is based on an accurate history and physical examination (with the finding of carotid bruits), a complete neurologic examination, a brain scan, an encephalogram and an angiogram. Recently the Holter technique for continuous 24-hour electrocardiographic monitoring has been used as a diagnostic aid in these problem cases. Severe bradycardia, sick sinus syndrome, tachy-brady syndrome, recurrent tachycardia and heart block have been found to be the cause of the central-nervous-system symptoms in aged atherosclerotic patients. Correction with anti-arrhythmia drugs and pacemakers, with or without carotid endarterectomy, has been highly successful. Data are presented on 204 patients tested by Holter monitoring over a 2.5-year period in a small community hospital; 6 cases are illustrated in detail. The Holter monitor is a valuable tool in evaluating the patients with cerebrovascular insufficiency.

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PubMed2001

Isolated petrous carotid stenosis and transient ischemic attack.

Although anterior circulation transient ischemic attacks (TIAs) tend to be more common in patients with extra- cranial carotid arterial disease than in those with intracranial carotid or middle cerebral arterial disease, the authors recently encountered 4 patients with both recurrent, stereotypical TIAs as well as isolated stenosis of their petrous internal carotid artery (ICA). While the gold standard for establishing the diagnosis of intracranial large-artery disease has always been conventional angiography, magnetic resonance angiography changes, confirmed with intra-arterial digital subtraction angiography in 2 of these patients, were quite sufficient to define the occlusive disease in each of the cases. Petrous ICA stenosis is not uncommon, but it has often been overshadowed by the search for extracranial ICA disease that might be amenable to surgical reconstruction.

Carotid Artery, Internal↗

PubMedDate not supplied

Anticoagulant vs anti-platelet therapy as prophylactic against cerebral infarction in transient ischemic attacks.

156 patients with transient ischemic attacks (TIA) or reversible ischemic neurological deficit (RIND) were given prophylactic anticoagulant (AC) treatment against cerebral infarction in a prospective multicenter study from 5 hospitals in southern Sweden. After 2 months of AC treatment, 135 patients remained in the study and were randomized into 2 groups; one continued with AC treatment and one changed to anti-platelet therapy. The patients were followed for 12 months. No significant difference was seen between the 2 groups but 3 completed cerebral infarctions occurred during anti-platelet therapy against one during AC treatment. One cerebral hemorrhage was seen during AC treatment. All completed strokes occurred in men who initially had carotid symptoms. The number of patients with TIA/RIND was somewhat higher in the anti-platelet group whereas myocardial infarctions occurred more often during AC treatment. Compared to the natural history of untreated TIA/RIND both treatments were found to have a prophylactic effect against cerebral infarction.

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PubMed2004

Transcranial magnetic stimulation in patients with transient ischemic attacks.

BACKGROUND: By definition, transient ischemic attacks (TIAs) do not leave a neurological deficit beyond 24 hours after onset. However, a subgroup of TIA patients is characterized by persistent perfusion defect on single photon emission computed tomogram or infarction on brain computerized tomogram and magnetic resonance imaging. Here, we applied transcranial magnetic stimulation (TMS) to study whether TIA could produce persistent subclinical dysfunction for more than 24 hours. METHODS: The study included 23 TIA patients who had the criteria of hand weakness as one of their clinical manifestations. TMS was done twice in each TIA patient. The first time was during the period of 24-48 hours after onset and the second 7 days after onset. We studied the cortical motor threshold, the latencies and the amplitudes of the motor evoked potentials, the central motor conduction time, and the cortical silent period at the intensity of 1.5 times motor threshold with maximal voluntary isometric contraction. The recording was at the first dorsal interosseous muscle. RESULTS: There was no significant difference between the whole group of TIA patients and normal control. However, in the subgroup of TIA patients who had hand weakness more than 1 hour, they had increased motor threshold and prolonged cortical silent period during the first test. Both improved 1 week after onset. On the contrary, in TIA patients who had hand weakness less than 1 hour, their data were all within normal limits during the first and the second studies. CONCLUSIONS: Our results indicate that the motor function of TMS study will recover to full if the motor symptoms subside within 1 hour in TIA patients. Subclinical motor deficits may persist in TIA patients who have motor symptoms more than 1 hour.

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PubMed2002

Hemodynamic and metabolic changes in transient ischemic attack patients: a magnetic resonance angiography and (1)H-magnetic resonance spectroscopy study performed within 3 days of onset of a transient ischemic attack.

BACKGROUND AND PURPOSE: We investigated whether patients with transient ischemic attack (TIA) have systemic low flow to the brain or an abnormal intracranial flow distribution caused by an abnormal anatomy of the circle of Willis. Furthermore, we investigated whether metabolic changes were present in the brain. METHODS: Forty-four patients with clinically diagnosed TIA were prospectively included in our study. Clinical and neurological data were compiled. MR imaging; quantitative flow measurements of the internal carotid, middle cerebral, and basilar arteries; MR angiography of the circle of Willis; and (1)H-MR spectroscopy were performed in all patients within 3 days of onset of symptoms. RESULTS: Compared with control subjects, TIA patients did not have altered flow volume in any of the arteries and had normal flow distribution through the circle of Willis. In TIA patients, the N-acetylaspartate (NAA)/choline ratio in noninfarcted regions was significantly decreased in the symptomatic hemisphere (1.73+/-0.16) compared with the asymptomatic hemisphere (1.84+/-0.19, P<0.05) and control subjects (1.90+/-0.17, P<0.001). In the symptomatic hemisphere, the lactate/NAA ratio was significantly increased (0.04+/-0.08) compared with control subjects (0.00+/-0.01, P<0.05). Patients with a history of prior TIA had a significantly decreased NAA/choline ratio in both the symptomatic (P<0.05) and asymptomatic (P<0.05) hemispheres compared with TIA patients without a prior TIA. CONCLUSIONS: TIA patients have neurological deficits that are transient; however, metabolic damage to the brain is present up to 3 days after the onset of the symptoms. These metabolic changes are not restricted to the symptomatic hemisphere or to areas close to ischemic lesions.

Adult↗

PubMed1995

Vitamin E plus aspirin compared with aspirin alone in patients with transient ischemic attacks.

One hundred patients with transient ischemic attacks, minor strokes, or residual ischemic neurologic deficits were enrolled in a double-blind, randomized study comparing the effects of aspirin plus vitamin E [0.4 g (400 IU)/d; n = 52] with aspirin alone (325 mg; n = 48). The patients received study medication for 2 y or until they reached a termination point. Preliminary results show a significant reduction in the incidence of ischemic events in patients in the vitamin E plus aspirin group compared with patients taking only aspirin. There was no significant difference in the incidence of hemorrhagic stroke although both patients who developed it were taking vitamin E. Platelet adhesion was also measured in a randomized subgroup of both study populations by using collagen III as the adhesive surface. There was a highly significant reduction in platelet adhesiveness in patients who were taking vitamin E plus aspirin compared with those taking aspirin only. Measurement of alpha-tocopherol concentrations confirmed compliance of the patients with the medication schedule, showing a near doubling of serum concentrations of alpha-tocopherol. We concluded that the combination of vitamin E and a platelet antiaggregating agent (eg, aspirin) significantly enhances the efficacy of the preventive treatment regimen in patients with transient ischemic attacks and other ischemic cerebrovascular problems.

Adult↗

PubMed2004

Transient ischemic attacks: Part I. Diagnosis and evaluation.

Transient ischemic attack is no longer considered a benign event but, rather, a critical harbinger of impending stroke. Failure to quickly recognize and evaluate this warning sign could mean missing an opportunity to prevent permanent disability or death. The 90-day risk of stroke after a transient ischemic attack has been estimated to be approximately 10 percent, with one half of strokes occurring within the first two days of the attack. The 90-day stroke risk is even higher when a transient ischemic attack results from internal carotid artery stenosis. Most patients reporting symptoms of transient ischemic attack should be sent to an emergency department. Patients who arrive at the emergency department within 180 minutes of symptom onset should undergo an expedited history and physical examination, as well as selected laboratory tests, to determine if they are candidates for thrombolytic therapy. Initial testing should include complete blood count with platelet count, prothrombin time, International Normalized Ratio, partial thromboplastin time, and electrolyte and glucose levels. Computed tomographic scanning of the head should be performed immediately to ensure that there is no evidence of brain hemorrhage or mass. A transient ischemic attack can be misdiagnosed as migraine, seizure, peripheral neuropathy, or anxiety.

Diagnosis, Differential↗

PubMed2006

The incidence of sleep apnea in patients with stroke or transient ischemic attack.

Disorders of breathing during sleep are defined as cessation or reduction of air flow thorough the upper airway, accompanied by a decrease of oxygen saturation. The results of many studies underline the association between sleep-disordered breathing (SDB) and cerebrovascular disorders. SDB, mostly obstructive sleep apnea syndrome (OSAS), is believed to be an independent risk factor of stroke and is related to poor outcome and increased long-term stroke mortality. The present study evaluated the frequency of SDB in patients with stroke or transient ischemic attack transient ischemic attack. We studied 43 patients (mean age 68.5 +/-11.0), which included 35 males and 8 females, with acute stroke (n=37) and transient ischemic attack (n=6). The assessment included body mass index (BMI), age, cardiovascular risk factors, and localization of stroke. All patients underwent all-night screening for SDB with a portable 8-channel recorder. The apnea/hypopnea index (AHI) for the whole group was 13.3 +/-15.2. AHI <5 was found in 16 patients. Overall, SDB was present in 27 (62.8%) patients with stroke and transient ischemic attack, stratified into those with AHI 5-10, (10 patients), 10-20 (8 patients), and AHI>20 (9 patients). In 15 patients, there was an increase in AHI >or=5 on assuming the supine position. The patients' mean BMI was 27.8 +/-4.7. The analysis of BMI, age, and localization of stroke was not sufficient to identify patients with high risk for SDB. We submit that overnight screening for SDB should be routinely performed in every patient after stroke and transient ischemic attack and it should become a diagnostic tool in neurological departments.

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PubMed2000

Do transient ischemic attacks have a neuroprotective effect?

OBJECTIVE: To determine whether TIAs have a neuroprotective effect. BACKGROUND: Ischemic tolerance or preconditioning, which protects the brain against stroke, has been demonstrated in animal models of cerebral ischemia. Because TIA may represent a clinical model of ischemic tolerance, patients with TIA before cerebral infarction (CI) may therefore have a better outcome than patients without TIA before CI. METHODS: A total of 2,490 patients admitted consecutively to a primary care center for first-ever CI in the anterior circulation were divided into two groups on the basis of the presence or absence of prior ipsilateral TIAs. Duration of TIA was classified into three groups (<10 minutes, 10 to 20 minutes, and >20 minutes). The severity of the neurologic picture on admission and functional disability after stroke were compared between patients with and without TIAs. RESULTS: A total of 293 (12%) of the 2,490 patients had prior ipsilateral TIAs before CI. Risk factors did not differ between patients with or without TIAs, whereas the topography and etiology of ischemic stroke did differ (p < 0.001). Patients without prior TIAs had a more severe clinical picture on admission, with a greater reduction of consciousness (p = 0.009). Patients with previous TIAs had a more favorable outcome than those without TIAs (67% versus 58%, p = 0.004). After adjustment for confounding variables, TIAs lasting 10 to 20 minutes were still associated with a favorable outcome (odds ratio, 1.98; 95% confidence interval, 1.27 to 3.08; p = 0.002). The interval between TIA and CI influenced the outcome (p = 0.007). CONCLUSIONS: This study suggests that ischemic tolerance may play a role in patients with ipsilateral TIAs before CI, allowing better recovery from a subsequent ischemic stroke.

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PubMed2000

Transient Ischemic Attack and Secondary Stroke.

Transient ischemic attack (TIA) is a clinical syndrome that has been shown to be a major risk factor for stroke. Patients with transient neurologic deficits of sudden onset that last less than 24 hours require prompt medical and neurologic evaluation for identifiable stroke risk factors. The appropriate treatment depends on the cardio- or neurovascular lesion that caused the TIA. Based on this evaluation, the optimal stroke prevention regimen in a person with TIA will vary from surgical repair of a stenotic carotid artery to daily aspirin use.

Journal Article↗

PubMed1985

[Point of view. Transient ischemic attacks. Is a reassessment needed?].

The clinical definition of transient ischemic attacks (TIAs), besides the ischemic pathogenesis is based (i) upon 24 h. duration and (ii) complete reversibility. The limit of 24 h. has been chosen arbitrarily and episodes clearing completely after more than 24 h. do exist. In addition TIAs lasting less than 5 min. would have a higher incidence of subsequent completed stroke. Complete reversibility has also been disregarded: ischemic attacks leaving slight neurological deficits or showing an hypodense area at CT scanning have been shown to have the same significance at TIAs. Different clinical definitions and classifications account for very different natural history features reported in the literature. Transient attacks may be conveniently assessed under the label of Reversible Ischemic Attacks (RIA) covering attacks of 24 h. duration (TIA) and attacks of more than 24 h. duration (Protracted Transient Ischemic Attacks. PTIA). Terms such a RIND or PRIND (Reversible Ischemic Neurological Deficit or Prolonged Reversible Ischemic Neurological Deficit) should be disregarded since they are too general terms covering both cases with 24 and more than 24 h. duration. TIAs and PTIAs should be characterized by a complete clinical regression and normal CT, to avoid relevant wrong diagnostic statements (transient attacks in cases of lacunar stroke, hemorrhages, tumours); where clinical regression is partial and/or CT shows low attenuation areas the case should be labelled as one with partial non progressing stroke (PNS) or minor stroke. The question however arises whether TIA, PTIA or PNS significantly differ from each other from the clinical, prognostic and therapeutic standpoint or, on the contrary, any attempt to differentiate them on these grounds should be considered futile as suggested be Caplan (1983).(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis, Differential↗

PubMed1986

Computerized tomographic abnormalities in patients with hemispheric transient ischemic attacks.

In 100 patients with transient ischemic attacks, correlations between clinical features and CT findings were analyzed. In 77 patients, CT scans were normal. Five percent had mass lesions and 18 had vascular lesions (ischemia, infarction, hematoma) delineated by CT. In two patients whose CT showed a hypodense lesion indicating cerebral infarction, clinical and CT worsening followed carotid surgery. In six patients with isodense enhancing lesions indicating ischemia, there was no clinical or CT deterioration after operation.

Adult↗

PubMed2005

Perfusion MRI abnormalities in speech or motor transient ischemic attack patients.

BACKGROUND AND PURPOSE: Transient ischemic attack (TIA) patients may deteriorate rapidly. MRI is being increasingly used to assess such patients. One possible mechanism of neurological worsening is the presence of perfusion abnormalities. We sought to identify what proportion of TIA patients had evidence of perfusion abnormalities on MRI. METHODS: TIA patients were prospectively enrolled and had a MRI completed as soon as possible. The images were assessed for the presence of perfusion abnormalities. RESULTS: Sixty-nine TIA patients were enrolled, and 62 had perfusion imaging. In 56 patients (81%), the symptoms had resolved before imaging. In 21 patients (33.9%), there was evidence of a perfusion abnormality defined by relative mean transit time delay. In 12 patients (19.4%), the perfusion abnormality was present despite having complete resolution of neurological symptoms. We found no relationship between the presence of a perfusion abnormality and the clinical outcome. CONCLUSIONS: A proportion of TIA patients have perfusion abnormalities evident on MRI.

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PubMed1990

Chinese patients with transient ischemic attacks.

In 123 cases of transient ischemic attacks, 72 were followed up for 22 years. The percentage of complete stroke was 46.5% and the fatality rate 47.9%. Causes of death, survival rate by life table, limitation of indication of neurovascular surgical operation and rehabilitation of survived patients were studied. The causes of death were mainly cerebral strokes. The long-term follow-up showed that the range for neurovascular surgical operation was limited to only 17.9%. The 95% confidence interval of the 20-year survival rate was 17.7-53.6%. Ninety-four, 48 and 44 cases were examined by B-mode Doppler tomography, cerebral CT scanning and echocardiography, respectively.

Adult↗

PubMed1993

Trial of secondary prevention with atenolol after transient ischemic attack or nondisabling ischemic stroke. The Dutch TIA Trial Study Group.

BACKGROUND AND PURPOSE: beta-Blockers prevent vascular events in patients after myocardial infarction and lower blood pressure, the main risk factor for stroke. Hence, we assessed the effects of atenolol on the occurrence of death from vascular causes, stroke, or myocardial infarction and on blood pressure in patients after a transient ischemic attack or nondisabling ischemic stroke. METHODS: In a double-blind, placebo-controlled randomized clinical trial we studied the occurrence of the outcome event death from vascular causes, nonfatal stroke, or nonfatal myocardial infarction and the outcome event fatal or nonfatal stroke as well as blood pressure on follow-up. A total of 1,473 aspirin-treated patients with transient ischemic attack or nondisabling ischemic stroke were randomized to 50 mg atenolol daily or placebo. The mean follow-up was 2.6 years. RESULTS: Patients on atenolol had a risk of 97/732 (13.3%) for the combined outcome event versus a risk of 95/741 (12.8%) for those on placebo (adjusted hazard ratio, 1.00; 95% confidence interval, 0.76-1.33). The adjusted hazard ratio for fatal or nonfatal stroke was 0.82 (95% confidence interval, 0.57-1.19). More patients on beta-blocker (153) reported adverse effects than on placebo (103). At the first follow-up visit after randomization (median at 4 months) systolic blood pressure in the atenolol group had dropped by 8.0 mm Hg compared with 2.2 mm Hg in the placebo group (difference, 5.8 mm Hg; 95% confidence interval, 2.9-8.6 mm Hg). For diastolic blood pressure this difference was 2.9 mm Hg (95% confidence interval, 1.5-4.4 mm Hg). CONCLUSIONS: Our data neither confirm nor rule out that atenolol prevents important vascular events in patients after transient ischemic attack or nondisabling ischemic stroke, given the modest effect on blood pressure, the restrictions in patient selection, and the limited number of patient-years.

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PubMed1989

A comparison of risk factors and prognosis for transient ischemic attacks and minor ischemic strokes. The Oxfordshire Community Stroke Project.

In a community-based study of transient ischemic attack and stroke, we identified 184 cases of transient ischemic attack and 213 cases of first-ever minor ischemic stroke. A comparison of age, sex, and prevalence of coexistent vascular diseases and risk factors revealed no major differences between the two groups. The risk of further stroke and of further stroke and/or death was greater in patients with minor ischemic stroke although the difference was significant only for the latter. The apparent differences in prognosis could largely be accounted for by the favorable prognosis of patients with amaurosis fugax among those with transient ischemic attack. Although for some purposes it may be useful to distinguish transient ischemic attacks from minor ischemic strokes, the similarity of the two groups suggests that in many situations, including in clinical trials of treatments for the secondary prevention of strokes, the arbitrary distinction between them could be dispensed with.

Adult↗

PubMed1998

Differentiation between transient ischemic attack and ischemic stroke within the first six hours after onset of symptoms by using 99mTc-ECD-SPECT.

The aim of this study was to define the accuracy of 99mTc-ethyl cysteinate dimer-single photon emission computed tomography (99mTc-ECD-SPECT) in distinguishing transient ischemic attack from completed ischemic stroke at early stages after the onset of symptoms. In a prospective study we examined 82 patients within 6 hours after the onset of symptoms (neurologic deficit caused by middle cerebral artery ischemia) using both 99mTc-ECD-SPECT and computed tomography (CT). The follow-up was based on Scandinavian Stroke Scale (SSS) 24 hours and 5-7 days, as well as on CT 7 days, after the event. SPECT evaluation was performed both visually and using semiquantitative region-of-interest (ROI) analysis. According to visual SPECT analysis, on admission 59 of 82 patients had activity deficits in the symptomatic hemisphere. After 7 days, all these patients had neurologic symptoms (SSS 28 +/- 12 points), caused by a cerebral infarction as evidenced with CT. Twenty-three of 82 patients displayed no early activity deficit despite clinical symptoms. None of these patients had neurologic symptoms after 7 days (indicating transient ischemic attack or prolonged reversible ischemic neurologic deficit). In the semiquantitative SPECT analysis, all patients had abnormal count densities in the respective ROI (activity < 90% compared with the contralateral side). All patients with transient ischemia (n = 23) had count rate densities more than 70% of the respective contralateral ROI, whereas all patients with subsequent infarction (n = 59) had values < 70%. Use of 99mTc-ECD-SPECT allows transient ischemia to be distinguished from ischemic infarction using relative regional activity thresholds within the first 6 hours after onset of symptoms.

Adult↗